These triggers decreased angiogenic factors, such as Placenta Growth Factor (PlGF), and increased antiangiogenic factors like soluble FMS-like tyrosine kinase-1 (sFlt-1), disrupting endothelial integrity, contributing to the clinical manifestations of PE, including proteinuria, hypertension, and end-organ damage [8, 9]. This evidence concerns the gene PGF and hypertensive disorder.